Kristin V Reinertsen1, Olav Engebraaten2, Jon H Loge3, Milada Cvancarova4, Bjørn Naume2, Erik Wist2, Hege Edvardsen5, Elisabeth Wille6, Trine Bjøro7, Cecilie E Kiserud8. 1. National Advisory Unit on Late Effects after Cancer Treatment, Oslo University Hospital, Oslo, Norway; Department of Oncology, Oslo University Hospital, Oslo, Norway. Electronic address: kvr@ous-hf.no. 2. Department of Oncology, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway. 3. Department of Oncology, Oslo University Hospital, Oslo, Norway; Department of Behavioral Sciences in Medicine, University of Oslo, Oslo, Norway. 4. National Advisory Unit on Late Effects after Cancer Treatment, Oslo University Hospital, Oslo, Norway; Oslo and Akershus University College of Applied Sciences, Faculty of Health Sciences, Oslo, Norway. 5. Department of Genetics, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway; Abbvie AS, Fornebu, Norway. 6. Department of Oncology, Oslo University Hospital, Oslo, Norway. 7. Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway; Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway. 8. National Advisory Unit on Late Effects after Cancer Treatment, Oslo University Hospital, Oslo, Norway.
Abstract
CONTEXT: Chronic fatigue (CF) in breast cancer (BC) survivors is multifactorial and may be caused by immune activation triggered by BC or its treatment. In the Neoadjuvant Avastin in Breast Cancer study, BC patients received neoadjuvant chemotherapy (FEC100→taxane) ± bevacizumab, a monoclonal antibody with fatigue as a potential side effect. OBJECTIVES: To examine fatigue levels and prevalence of CF before and during chemotherapy and at follow-up, and their associations with C-reactive protein (CRP) and clinical variables. METHODS:Eighty-four HER2-negative patients with cT2-4N0-3M0 BC responded to questionnaires and had CRP measured before treatment (T0), after FEC100 (T1), after taxanes before surgery (T2), and at two-year follow-up (T3). RESULTS: The prevalence of CF increased from 8% at T0 to 36% at T3, P < 0.0001. Fatigue levels peaked during chemotherapy from 12.0 at T0 to 20.0 at T2, and declined to 16.7 at T3, P < 0.001. Women with CF at T3 had higher fatigue levels at T0, T2, and T3 than those without CF (P ≤ 0.01). Psychological distress (P = 0.03) and pain (P = 0.04) at T3 were associated with CF at T3. Only psychological distress remained a significant predictor in multivariate analysis. CRP increased from T0 to T1 (P < 0.01) and declined to baseline values at T3, but changes were not associated with bevacizumab treatment. No association was found between bevacizumab or CRP, and fatigue levels or CF. CONCLUSION: Neither bevacizumab treatment nor low-grade systemic inflammation as measured by CRP was associated with the increased fatigue levels and raised prevalence of CF, observed during and after BC therapy. Increased fatigue levels at baseline and psychological distress at T3 were associated with CF at T3.
RCT Entities:
CONTEXT: Chronic fatigue (CF) in breast cancer (BC) survivors is multifactorial and may be caused by immune activation triggered by BC or its treatment. In the Neoadjuvant Avastin in Breast Cancer study, BC patients received neoadjuvant chemotherapy (FEC100→taxane) ± bevacizumab, a monoclonal antibody with fatigue as a potential side effect. OBJECTIVES: To examine fatigue levels and prevalence of CF before and during chemotherapy and at follow-up, and their associations with C-reactive protein (CRP) and clinical variables. METHODS: Eighty-four HER2-negative patients with cT2-4N0-3M0 BC responded to questionnaires and had CRP measured before treatment (T0), after FEC100 (T1), after taxanes before surgery (T2), and at two-year follow-up (T3). RESULTS: The prevalence of CF increased from 8% at T0 to 36% at T3, P < 0.0001. Fatigue levels peaked during chemotherapy from 12.0 at T0 to 20.0 at T2, and declined to 16.7 at T3, P < 0.001. Women with CF at T3 had higher fatigue levels at T0, T2, and T3 than those without CF (P ≤ 0.01). Psychological distress (P = 0.03) and pain (P = 0.04) at T3 were associated with CF at T3. Only psychological distress remained a significant predictor in multivariate analysis. CRP increased from T0 to T1 (P < 0.01) and declined to baseline values at T3, but changes were not associated with bevacizumab treatment. No association was found between bevacizumab or CRP, and fatigue levels or CF. CONCLUSION: Neither bevacizumab treatment nor low-grade systemic inflammation as measured by CRP was associated with the increased fatigue levels and raised prevalence of CF, observed during and after BC therapy. Increased fatigue levels at baseline and psychological distress at T3 were associated with CF at T3.
Authors: Joseph M Gullett; Ronald A Cohen; Gee Su Yang; Victoria S Menzies; Robert A Fieo; Debra L Kelly; Angela R Starkweather; Colleen K Jackson-Cook; Debra E Lyon Journal: Psychooncology Date: 2019-03-14 Impact factor: 3.894
Authors: Alexander Fosså; Knut Halvor Smeland; Øystein Fluge; Karl Johan Tronstad; Jon Håvard Loge; Øivind Midttun; Per Magne Ueland; Cecilie Essholt Kiserud Journal: PLoS One Date: 2020-01-10 Impact factor: 3.240
Authors: Fay Wright; Kord M Kober; Bruce A Cooper; Steven M Paul; Yvette P Conley; Marilyn Hammer; Jon D Levine; Christine Miaskowski Journal: Support Care Cancer Date: 2020-01-20 Impact factor: 3.603